title: Effects of glucagon-like peptide-2 on bacterial translocation in rat models of colitis.
abstract: OBJECTIVE
  The aim of this trial was to study the role of glucagon-like peptide-2 in reducing bacterial translocation by virtue of its anti-inflammatory effects and ability to decrease intestinal permeability in rat models of inflammatory bowel diseases. On the basis of our results and those of other recent studies, we suggest a new treatment modality for colitis. To our knowledge, this is the first study of the effectiveness of glucagon-like peptide-2 on bacterial translocation, in treating an experimental colitis model.
  
  
  METHODS
  Rats were randomized into 3 groups of 7 rats each-the control group, colitis group, and treatment group. On the 7 th day after induction of colitis, the levels of tissue myeloperoxidase, serum tumor necrosis factor-alpha, and plasma endotoxin were measured. Tissue samples were obtained from the liver, spleen, and mesenteric lymph nodes for evaluating bacterial translocation.
  
  
  RESULTS
  Bacterial translocation in samples of the liver, spleen, mesenteric lymph nodes, and portal and systemic blood obtained from the treatment group was lower than that in samples obtained from the colitis group (p < 0.05). The levels of tissue myeloperoxidase, serum tumor necrosis factor-alpha, and plasma endotoxin in the treatment group were significantly lower than those in the colitis group (p < 0.05).
  
  
  CONCLUSIONS
  In experimental colitis models, which were induced using trinitrobenzene sulfonic acid in ethanol, glucagon-like peptide-2 treatment reduced inflammation and bacterial translocation from the intestinal mucosa. Our results indicate that glucagon-like peptide-2 is a potential agent for treating colitis; however, extensive trials are needed to confirm our results.
authors.affiliation: Department of General Surgery, Viranflehir State Hospital, Viranşehir, Şanlıurfa, Turkey.
authors.forename: Bülent
authors.initials: B
authors.lastname: Halaçlar
authors.forename: Aybala
authors.initials: A
authors.lastname: Ağaç Ay
authors.forename: Alper Celal
authors.initials: AC
authors.lastname: Akcan
authors.forename: Ahmet
authors.initials: A
authors.lastname: Ay
authors.forename: Bahadır
authors.initials: B
authors.lastname: Öz
authors.forename: Engin
authors.initials: E
authors.lastname: Arslan
mesh_terms: D000818:Animals; D018988:Bacterial Translocation / Q000187:drug effects*; D003092:Colitis / Q000139:chemically induced / Q000188:drug therapy* / Q000382:microbiology*; D003106:Colon / Q000187:drug effects / Q000382:microbiology / Q000473:pathology; D004195:Disease Models, Animal; D004731:Endotoxins / Q000097:blood; D053767:Glucagon-Like Peptide 2 / Q000494:pharmacology*; D008297:Male; D009195:Peroxidase / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D016896:Treatment Outcome; D014302:Trinitrobenzenesulfonic Acid / Q000633:toxicity; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D004731:Endotoxins; D053767:Glucagon-Like Peptide 2; D014409:Tumor Necrosis Factor-alpha; D014302:Trinitrobenzenesulfonic Acid; D009195:Peroxidase